Paper
An adamantane derivative (N-N'(1-adamantil)-ethylene diamine dibromide) induced automaticity in the ventricular myocardium of the frog.
Published 1981 · J. Mészáros, T. Kovács, A. Dinya
Acta physiologica Academiae Scientiarum Hungaricae
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Abstract
The effect of an adamantane derivative (N-N'(1-adamantil)-ethylene diamine dibromid; AED) on the transmembrane potentials and contractile activity of isolated electrically driven frog ventricular strips were studied. The effect of AED on the 42K efflux in ventricular muscle rings was also investigated. AED at a concentration of 10(-3) M markedly reduced the rate of depolarization and prolonged the duration of action potential. The resting potential was shifted to less negative potential ranges and pacemaker-like action potentials appeared within 10 minutes of exposure to drug. AED was found to exert an enhancing effect on the contractile force of the frog ventricular muscle. The slow Ca2+-channel blocked D-600 was able to abolish completely the AED-induced automaticity, while the beta-adrenoceptor blocker pindolol failed to prevent this action. The pacemaker activity was reduced by increasing external K+ concentration. AED markedly reduced the 42K efflux in ventricular muscle rings. In conclusion, the AED was shown to be able to induce automaticity by decreasing the outward movement of potassium ions and by depolarizing the cell membrane.
In Vitro StudyThe adamantane derivative AED induces automaticity in frog ventricular muscle by decreasing potassium ion outflow and depolarizing the cell membrane.
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